Archive for the ‘Training’ Category

The Zone is that magical state in which running seems almost effortless. When it descends upon you, it feels like a state of grace bestowed by Hermes, the swift-footed messenger who could effortlessly outrun all other Olympian gods. Hermes was also a cunning trickster, and his gift cannot be taken for granted. The exact nature of the state of mind and brain that facilitates this magical experience remains unknown. Nonetheless as outlined in my previous post, neuroscience has revealed many factors that play a part.

These include the endocannabinoids that are released during exercise. Endocannabinoids are analgesic and create a sense of euphoria. They interact in a complex manner with the neurotransmitter, dopamine, which mediates the experience of reward, and plays a key role in the learning of patterns of behaviour. The relevant neural circuits connect the frontal cortex, limbic system and basal ganglia. While the interactions within these circuits that mediate the experience of the Zone appear to be subtle and complex, there is little doubt that these circuits can be trained.

Neurons that fire together

In recent years it has become clear that in general brain circuits are far more adaptable, even in adult life, than had hitherto been recognised. One of the earliest indicators of this plasticity of the adult human brain was provided by Eleanor Maguire’s demonstration that London taxi drivers have an increased amount of grey matter in the posterior hippocampus, a part of the limbic system that is engaged during spatial navigation. For our present purpose, it is crucial to note that in those days, London taxi drivers spent several years learning the layout of the streets of London to qualify for a cab-driver’s licence. Subsequent brain imaging studies have confirmed that intense practice of various motor skills (such as juggling) and cognitive skills (such utilizing material maintained in short term memory) leads to an increase in the amount of grey matter in the brain regions engaged during those activities.

Many details of the molecular mechanism by which neural pathways are strengthened are known. It is a process known as long term potentiation (figure 1). When a signal is transmitted across the synapse connecting one nerve cell with the next one in the circuit, it not only results in the onward transmission of the electrical signal, but also sets in train a series of chemical events in the receiving nerve cell. Those chemical events lead to an immediate increase in the efficiency with which the synapse can transmit signals and also to the transcription of DNA to produce proteins that produce long-lasting changes in the strength of the connection. The delineation of this process in recent years has confirmed the speculation of the Canadian psychologist, Donald Hebb, in his book, the Organization of Behaviour, written in 1949. Hebb proposed that ‘neurons that fire together wire together’.

Figure 1. Neurons that fire together wire together. An incoming electrical signal releases a transmitter molecule (glutamate) into the space between the nerve endings. The glutamate binds to an AMPA receptor on the surface of the receiving neuron, changing its shape allowing the flow of ions. The electrical a potential changes, thereby transmitting the electrical signal to the receiving neuron. The change of potential also expels the blocking magnesium ion from the NMDA receptor. Calcium ions flow inwards and initiate a series of chemical events that make the synapse more efficient in both the short term and also the long term.

The implication is that if we wish to strengthen a particular skill we need to practice that skill persistently. The converse is also true: if we practice the relevant activity in a counter-productive manner we will strengthen the counter-productive pattern of brain activity. What is the right way to develop the circuit that facilitates the experience of the Zone, and what is the wrong way?

The Central Governor

Tim Noakes concept to the central governor provides a clue to the right way and the wrong way. According to Noakes, our brain creates a sense of fatigue that causes us to restrict our involvement in a demanding exercise when the cumulative signals for the body about our metabolic state, indicate that we are approaching our limit. But as anyone who has sprinted at the end of a marathon despite feeling almost overwhelming fatigue with a mile to go knows, the governor is far too conservative. Perhaps in prehistoric times, when food supply was uncertain and our forebears needed conserve reserve fuel to escape from an unpredictable predator, their glucose-dependent brains learned to set the governor conservatively. Our forebears did of course have an over-ride mechanism: the adrenaline system could dramatically reset the governor’s limits in case of emergency. We too can utilise adrenaline to reset the governor during a race, but in a long race, too much reliance on adrenaline is damaging. A better strategy is to train the brain in manner that resets the governor, and delays the onset of fatigue. We need to reframe the experience of effort when running: rather than perceiving effort as fatiguing or painful, we need to perceive effort as satisfying, even perhaps exhilarating.

Confidence

How do we do this? The first thing is to develop thought patterns that engender confidence. Grandmothers’ wisdom tells us that nothing succeeds like success. In more recent times, the psychologist Martin Seligman has developed an approach to building resilience based on Positive Psychology. His Mental Resilience Program is currently employed by the US military to produce mental toughness in soldiers. Modern neuroscience confirms that during challenging tasks, confident individuals who engage areas of the medial frontal cortex more effectively outperform individuals who do so less effectively. If two athletes have identical aerobic capacity and efficiency, the one who believes he/she will win will almost certainly be the winner.

Perception is more important than reality. In fact pessimistic people generally tend to see the world as it really is. Freud famously remarked that only depressed people see the world as it really is, and much subsequent evidence has proven him correct. But we function better with a self-reinforcing positive bias. Nonetheless Positive Psychology is not merely about telling yourself you will win. We are not so easily fooled. We need to acquire the habits of optimistic thinking. Optimistic thinking focuses on the specific details of the experience rather than overgeneralization and self-defeating prediction. We need to train hard and give ourselves due credit for success in achieving our training goals, while identifying the specific problem when we fail to reach the target we set.

In particular, we need to frame challenges in terms of Albert Ellis’s ABC model: C (emotional consequences) stem not directly from A (adversity – e.g, the sensation of shortness of breath) but from B (one’s beliefs about adversity). In dealing with the A’s we need to learn to separate B’s—heat-of-the-moment over-generalised reaction to the situation (“I’m a failure”)—from C’s, the emotional consequences generated by those thoughts (“I cannot maintain this pace” is replaced by “I am breathing intensely; I’m running powerfully”). Then move on to D; dispel the fear of failing. There is no need to abolish negative thoughts and emotions entirely. Identify their source. Once you have given a negative thought a name, your brain can cope with it more successfully. We need to build the sense that we are in control of ourselves; our thoughts and emotions.

Breathing

I find that it is very helpful to focus specifically on breathing, during both training and racing. Start with awareness of breathing; then relate breathing to footfall as this promotes controlled breathing. I find focus on arm swing is also useful: the brain programs whole movements rather than single muscle contractions. The brain nonetheless devotes more processing resources to arm and hand than to leg and foot. Our brain readily links arm movement to leg movement; we can enhance this link in our brain by practicing the focus on arm swing while being aware of footfall. I think a firm down/back stroke of the arm promotes a strong drive in the second half of stance that is associated with rhythmic breathing.

However do not expect to be able to focus on all of these things at once without practice. It took several years before I could focus on these things in a relaxed confident manner. Do not get tense if you cannot focus on everything. Find what you can focus on comfortably and aim for a relaxed focus on this. When you are in the appropriate confident relaxed state time seems to expand to accommodate the events you are attending to.

I learned these aspects of mental focus long before mindfulness became popular. However when the technique of mindfulness emerged into popular culture in recent years, I found the key aspects of mindfulness came easily – probably because I had developed those skills when running. Conversely, it is likely that acquiring mindfulness skills will help you to apply these techniques when running. Brain imaging studies demonstrate that mindfulness produces changes in functioning of the insula (figure 2), plausibly promoting constructive awareness of internal reactions ‘in-the-moment’.

Figure 2: The insula and limbic system. The insula lies in a fold of cortex hidden between the medial temporal lobe, containing the amygdala and hippocampus, and the deep grey nuclei. The insula mediates the interaction between sensory perception, thought and emotion.

Repetition

Whatever specific strategies work for you, you need to practice them repeatedly in every training session. You will build brain circuits that can sustain a mental state that is confident and in control in all circumstances. When Hermes smiles upon you, you will find yourself in that transcendental state in which you are running powerfully with minimal effort and no sense of fatigue.

Avoiding injury is one of the major goals of training for distance running. On account of the impact forces experienced at footfall on every stride, runners are uniquely prone to injury. However, effective strategies for preventing injury are elusive. In recent years, advocates of techniques such as Pose have claimed that injuries are largely due to poor running technique, and have promised that the problem can be overcome by proper technique. In particular, they have identified heel striking as a cardinal problem. However, there is very little evidence to support this claim. Others have advocated stretching during warm-up as a strategy to reduce risk of injury, though the evidence provides little support for this claim. Advocates of barefoot running have proposed that running shoes are the problem, but again there is little evidence to support the claim that running barefoot or in minimalist shoes reduces risk of injury. Conversely, the manufacturers of running shoes have placed blame on foot orientation problems such as over-pronation and claimed that motion control shoes can reduce this risk. Yet again, the evidence is slight, though at least one study had found that over-pronation is associated with increased risk of injury.

It is likely that a wide variety of factors contribute to injury in different individuals. Meta-analyses that pool the findings of many studies are only likely to identify risk factors that are common to many athletes. Two risk factors emerge consistently: a history of previous injury; and a large weekly volume of training. Lisa Callaghan has provided an up-to-date review of the evidence.

Prior injury

A history of previous injury might predispose to subsequent injury simply because the athlete has not corrected problems that contributed to the first injury. It is also possible that unsatisfactory recovery from the previous injury plays a role. Muscles, tendons and other connective tissues tear when subjected to force that exceed the limits of their resilience. A cardinal factor in the resilience of connective tissues is the elongated spring-like structure of collagen fibres, making them resilient against forces acting along the direction of the fibre. During the initial stages of repair following injury, collagen is laid down with random orientation providing a framework for tissue renovation, but full resilience requires remodelling such that the collagen fibres become aligned in the required direction. Therefore effective recovery requires early mobilization to promote the laying down of appropriately aligned fibres, perhaps augmented by slow stretching.

Training volume

Observational studies report that training volumes of 65 Km (40 miles) or more per week are associated with higher rates of injury [Fields et al;van Ghent et al]. In part these observations might simply reflect the greater duration of exposure to risk of injury, though it is likely that fatigue plays an important role. In particular fatigue impairs neuromuscular coordination increasing the likelihood of poor coordination between different types of muscles fibres within a muscle and poor coordination between muscles that act as agonists and antagonists, resulting in excessive local forces within tissues.

Polarized training

Simply limiting training volume is unlikely to be a satisfactory strategy for many runners, making it desirable to identify alternative strategies to reduce the damaging effects of fatigue. As the forces exerted increase with increasing pace, it might be expected that injury risk would be greater at faster paces. However the observation by Van Middelkoop and colleagues that among marathon runners, those who do interval training have a lower risk of knee injury raises an intriguing question. Could it be that interval training provides greater protection than training at somewhat lesser paces in the vicinity of lactate threshold? Interval training, in which short efforts at fast but sub-maximal pace are separated by recovery periods, tends to promote the development of neuromuscular coordination with relatively mild muscle fatigue. As discussed in my recent post, interval training is likely to promote a favourable balance between anabolic and catabolic hormones, leading to strengthening of tissues. In contrast, running for a sustained period at threshold pace might produce fatigue with the associated risky deterioration of neuromuscular coordination during the session, and also tip the balance towards the catabolic effects of cortisol, promoting subsequent breakdown of tissues.

Even more speculatively, the viscoelastic character of the musculotendinous unit might result in a peak risk of damage to muscles and tendons at threshold paces. Viscoelastic materials offer strong resistance to brief sudden onset forces but less resistance to sustained forces. Although force is greater at sprinting pace, time on stance decreases. At speeds above LT there is actually a decrease in the impulse acting through the foot at each step because the increased force is more than compensated by reduction in time on stance. The product of forces x time on stance actually decreases, as illustrated in figure 1 based on data from the study by Weyand and colleagues.

Figure 1. Upper panel: the average vertical force (expressed relative to body weight) during stance as a function of running speed. Lower panel: the vertical impulse (average force x duration of stance) transmitted through the leg during stance as a function of running speed.

Thus, it is possible that the risk of tissues tearing is actually less at sub-maximal paces substantially above LT than in the vicinity of LT. Nonetheless, it is crucial to prime the requisite neuromuscular coordination during the warm-up (for example by moderate intensity strides) and it is generally desirable to avoid absolutely maximal effort that taxes neuromuscular coordination to the limit, during training.

The other pole of polarised training is low intensity running. This has the potential to build resilience of the muscles, tendons and the other connective tissues engaged during running by repeated application of moderate forces. Provided training volume is built-up gradually and excessive fatigue is avoided, the risk of injury is low.

Conclusion

While the predisposing and precipitating factors causing running injuries remain controversial, consistent evidence indicates that a high weekly training volume increases the risk. In contrast, the observation that interval training provides some protection suggests that polarised training might diminish the risk. Observational evidence and also speculation based on principles of biomechanics and physiology suggest that high intensity sessions have the potential to build effective neuromuscular coordination, while low intensity training would be expected to enhance the resilience of muscles, tendons and other connective tissues with relatively little risk. Nonetheless, as with any type of training, it is important to build up the training load gradually, and to warm up for each session in a manner the primes the requisite neuromuscular coordination.

My previous post discussed evidence indicating that training in the vicinity of lactate threshold (LT) can lead to sustained elevation of cortisol which has the potential to damage to the neuromuscular system and suppress immune responses. In particular, the study by Balsalobre-Fernandez indicates that frequent training at or a little above lactate threshold is more damaging than a lesser amount of training at a higher intensity. This might be the key to understanding why a growing body of evidence favours polarized training, which includes a large volume of low intensity training, a small amount of high intensity training and a similarly small amount of threshold training, in preference to a training program with a higher proportion of threshold training.

As distance races from 5 Km to marathon are raced in vicinity of lactate threshold, pace at LT is a crucial determinant of performance. Enhancing the ability to delay the onset of lactic acid accumulation as pace increases is one of the key goals of training. The effectiveness of polarised training raises the question of how a program with only a small about of threshold training might nonetheless be effective in enhancing ability to minimise lactate accumulation.

Lactate accumulation might be minimised by decreasing the rate of production and /or increasing ability to remove it. The rate of production can best be minimised by increasing the capacity to generate energy aerobically, which in turn might be enhanced by increasing the capacity of aerobic enzymes in mitochondria and/or increasing delivery of oxygenated blood to muscles.

Developing Aerobic Capacity

While a large volume of low intensity running would be expected to increase the aerobic enzymes in slow twitch fibres, the more challenging question is how to enhance the aerobic capacity of fast twitch fibres. Low intensity running beyond the point of exhaustion of slow twitch fibres might help achieve this, but frequent very long runs create the risk of excessive stress. For many years followers of Arthur Lydiard’s approach to periodization, in which the base-building phase is almost exclusively devoted to relatively low intensity aerobic running, have maintained that when you bring speed work into the program, you halt the development of aerobic enzymes. The size of the engine is now fixed; the task of speed work is to tune this engine.

This claim was associated with a widespread belief that the acidity generated above LT prevented development of aerobic enzymes, and perhaps even damaged them. This belief is ill-founded. Extensive research into high intensity interval training (HIIT) in recent years has demonstrated that HIIT is a very efficient way to increase the capacity of aerobic enzymes. The available evidence indicates that HIIT achieves the enhancement of mitochondrial enzymes via the increasing the activity of the messenger molecule, PGC-1alpha, the same messenger as appears to mediate mitochondrial development in response to lower intensity endurance training

HIIT research is largely focussed on comparing high intensity training with low intensity training and has not so far investigated the potential benefits of a polarised approach. It would be anticipated that in a polarised approach the rate of gain in aerobic capacity would not be a rapid as with HIIT, but it is scarcely credible that diluting the high intensity session with low intensity sessions would abolish the aerobic gains of the high intensity sessions, provided there is adequate opportunity for recovery.

Not only does HIIT produce efficient development of aerobic enzymes, but it is also effective in enhancing the development of the enzymes that metabolise fats, thereby promoting the generation of energy from fat, a processes that does not generate lactate

With regard to increasing the supply of oxygenated blood to muscle, sprint interval training is as effective as endurance training in promoting development of capillaries. Although the effect of HIIT on development of cardiac output has been less thoroughly studied, it is noteworthy that the Gerschler’s rationale for the introduction of interval training was the stimulation of cardiac output. In his word interval training provides “a stimulus particularly powerful to reach the heart.”

Transport of lactate

The alternative approach to minimizing lactate accumulation is removal of lactate from muscle and blood. With regard to the relative efficacy of polarised training compared with threshold training, the important issue is whether or not this is better promoted by brief surges of intensive lactate production or by sustaining a moderate level of lactate. The mechanisms by which lactate is removed from muscle include the transport of lactate from fast twitch fibres, where it is produced, to slow twitch fibres, which have the capacity to metabolise the lactate; the transport to other organs such as heart muscle which are well adapted to metabolising lactate; or transport to the liver where the process of glycogenesis converts lactate to glucose and subsequent storage in the form of glycogen.

The transport of lactate across cell membranes is mediated via a set of transport molecules, the monocarboxylate transporters (MCTs) that transport lactate together with protons. Transport by MCT’s involves diffusion and the rate is determined by the transmembrane gradient of either lactate or acidity (protons). It is likely that under most conditions, lactate flux is determined mainly by the gradient produced by metabolism-driven uptake, while the availability of MCTs is rate-limiting only after the establishment of large transmembrane gradients. Therefore, the first goal in enhancing the capacity to clear lactate during distance running is enhancing the ability to metabolise lactate. In heart and slow twitch fibres, this is achieved by enhancing vascularization and aerobic enzyme activity. The evidence discussed above suggests that polarized training is an effective way to do this. Nonetheless, it is desirable to ensure that MCT’s are maintained at an adequate level. Because MCT-mediated transport is rate-limiting only in the presence of large transmembrane gradients, it would be expected that brief surges of lactate will be more effective in promoting development of MCTs than sustained moderate levels.

Buffering of acidity

The role of acidity in stimulating training effects is ambiguous. On the one hand rising acidity eventually halts metabolism in muscle, but on the other, some degree of stress is likely to be necessary to promote adaptation. Ingestion of sodium bicarbonate (baking soda) which neutralises acid has been shown to diminish the secretion of anabolic hormones, such as growth hormone, following intense exercise. Thus rise in acidity appears to facilitate at least some of the desired effects of training. In contrast, sodium bicarbonate ingestion augments the increase in activity of the messenger molecule PGC-1alpha in skeletal muscle during recovery from intense interval exercise in humans, and therefore might promote the development of mitochondria.

This raises the question of the role of natural buffering mechanisms in the blood. During intense exercise there is a transient rise in the body’s natural buffers, phosphate ions and bicarbonate ions, that helps neutralise the rise in acidity despite the rise in lactate concentration. Thus it is plausible that one of the advantages of interval training compared with threshold training is that the transient natural buffering during interval training allows more intense exercise and hence allows greater lactate production without excessive acidity. Perhaps this would act as a greater stimulus to PGC-1 Alpha activity and perhaps MCT production as well. On the other hand, natural buffering might diminish the potentially beneficial increase growth hormone activity. Overall, on account of the competing antagonistic effects, I doubt that buffering is an important adjunct to training. The issue is similar to the debate about the value of cold baths to reduce inflammation after training.

Nonetheless, the possibility that buffering might increase tolerance of lactate production, together with the substantial evidence for improved endurance performance in rats and humans, reviewed McNaughton and colleagues, has led to the proposal that bicarbonate doping might enhance race performance. I am intrinsically opposed to the ingestion of substances in marked excess of the amounts present in a normal healthy diet for the sake of enhancing performance, but some athletes might argue that provided it is not illegal it is acceptable. However, the dose required to produce an appreciable effect (20-30 gm) can cause vomiting or diarrhoea. I would regard this is too great a risk to take.

Long term improvement

It is clear that many of the physiological adaptations required to minimise the rate of accumulation of lactate can be achieved very efficiently by HIIT. This evidence undermines the principle that enhancement of the ability to handle lactate is achieved most effectively by specific training in the vicinity of LT.

Unfortunately, most of the HIIT research so far has focussed on the contrast of HIIT with lower intensity training, delivered over a time scale of several weeks. There is some evidence that the benefits of HIIT do plateau after a period of a few months. The study by Stoggl and Sperlich demonstrated that for athletes who have a history of regular training, polarised training produces greater benefits than either threshold training or predominantly high intensity training. It is plausible that the adaptations produced by HIIT can also be achieved, perhaps more gradually but with the potential for steady improvement over a prolonged period, by a polarised program. Hitherto there have been too few studies that have examined the development of physiological capacities such as aerobic enzymes, delivery of blood to muscle and the transport of lactate, during training programs sustained over a full season or longer.

Injury prevention

Injury is an issue of perennial importance to athletes. In general, muscle injury is likely if a large force is exerted unexpectedly, or if muscles are fatigued. Protection against injury is minimised by the strengthening promoted by anabolic hormones on the one hand, or diminished by the breakdown of tissues promoted by sustained elevation of catabolic hormones such as cortisol. In the next post in this series, I will address the question of whether injury is more or less likely with a polarised program than with threshold training.

In the early years of a runner’s career, almost any reasonably sensible training plan with a gradual build-up of training load will produce improvement. However, once a runner has reached a plateau of performance, the challenge is to identify the type of training that offers the best chance of further improvement. Races ranging from 5K to marathon are run at paces in the vicinity of lactate threshold (LT). Race performance is largely determined by the fact that as pace rises above lactate threshold, acid accumulates in muscles and blood, eventually resulting in an enforced slow-down. Thus, one of the major goals of training is increasing pace at lactate threshold, as this will allow increased race pace. The principle of specificity of training suggests that the optimum training program will include a large amount of running near lactate threshold to enhance capacity to prevent accumulation of acid. Indeed, this is the approach adopted by many recreational runners.

Polarized training

However, the evidence from examination of the training logs of elite endurance athletes, reviewed comprehensively in a lecture by Stephen Seiler in Paris in 2013, indicates that many elites adopt a polarised approach that places emphasis on the two extremes of intensity. There is a large amount of low intensity training (comfortably below LT) and an appreciable minority of high intensity training (above LT). Polarised training does also include some training near lactate threshold, but the amount of threshold training is modest; typically the proportions are 80% low intensity, 10% threshold and 10% high intensity.

As reviewed in my previous post on the topic, several scientific comparisons of training programs have demonstrated that for well-trained athletes who have reached a plateau of performance, polarised training produces greater gains in fitness and performance, than other forms of training such as threshold training on the one hand, or high volume, low intensity training on the other.

The specificity principle

Nonetheless many coaches and athletes who advocate specific training paces to achieve the various required adaptations required for distance running, maintain a firml belief that threshold training is the best way to increase the pace at lactate threshold, and should form a substantial component of a distance runner’s training program. Jack Daniels, doyen among coaches advocating specific paces for specific adaptations, has argued that because stress level rises rapidly at paces exceeding threshold there is a sweet spot in the vicinity of lactate threshold that achieves sufficient stress to promote adaptation while avoiding the danger of excessive stress.

Evidence from laboratory studies of rats appears to provide some support for this view. While it is necessary to be cautious in using evidence from studies of rats to inform training of humans, the basic physiology of rat muscle is similar to that of human muscle. They share with us an aptitude for running at aerobic paces. The evidence from the well-controlled systematic studies that are feasible in rats is potentially useful in establishing principles that apply across species. Dudley’s studies in which he measured changes in aerobic enzymes produced by a variety of different training intensities and durations in rats (all training for 5 days per week for 8 weeks) demonstrated that running beyond a certain duration produced no further increase in aerobic enzymes. Furthermore, the duration of running beyond which there was no further improvement is shorter at higher training intensity. This suggests that at any given intensity, training runs beyond a certain duration will produce no further increase in aerobic capacity though there might of course be other gains, for example increase resilience of bones, muscles, ligaments, tendons and also the mind. But there is also likely to be an increase in overall stress. At very high intensity the duration limit is so short that the overall gain in aerobic fitness is less than can be achieved by longer session at lower intensity. The greatest overall increase in aerobic enzymes in muscles with predominantly red (aerobic) fibres, was achieved by an intensity that led to maximum gain at around 60 minutes. Thus in Dudley’s rats, there appeared to be a sweet spot in intensity for optimum development of aerobic capacity. Although Dudley did not measure lactate levels, it is plausible that this intensity corresponds roughly to lactate threshold in humans.

Hormones and training

However even if we accept that Dudley’s studies support Jack Daniel’s argument for a sweet spot, it is crucial to note that Dudley assessed the effects of training over a total duration of only eight weeks. The important issue for the athlete who has reached a plateau is the likely consequences of training over a longer time-scale than 8 weeks. It is probable that the crucial issue is the balance between catabolic and anabolic effects of training. During a training session, the catabolic hormones cortisol and noradrenaline are released into the blood stream to mobilise body resources, especially glucose, required to meet the demands of training. The release of catabolic hormones also triggers the subsequent release of anabolic hormones, such as growth hormone, that promote repair and strengthening of body tissues. As training intensity rises above lactate threshold the release of catabolic hormones and the associated release of anabolic hormones increases sharply (as illustrated by Wahl and colleagues). Thus the potential stimulus triggering the benefits of training rises sharply as intensity exceeds lactate threshold. The accumulation of cortisol also increases with increased duration of running. For example, Cook and colleagues report that salivary cortisol increases steadily during a marathon, typically achieving a fourfold increase at 30 minutes after completion of the race compared with the level prior to the start.

While a transient rise in cortisol tends to be beneficial, sustained elevation of cortisol is potentially harmful because cortisol promotes the breakdown of body tissues. Cortisol levels in hair samples provide an indication of cortisol level sustained over a period of weeks or months. Skoluda et al measured cortisol levels in hair in a group of distance runners over a season. They reported that these runners had abnormally high cortisol levels over a prolonged period, raising the possibility of adverse sustained catabolic effects, including suppression of the immune system. Skoluda concluded that repeated physical stress of intensive training and competitive races is associated with potentially harmful sustained elevation of cortisol. However, they did not explicitly compare different training programs.

There is no published evidence of differences in medium or long term catabolic/anabolic balance between polarised training and threshold training. Furthermore, because gradual increase in training load leads to a blunting of the sharp rise in catabolic hormones produced by training in the vicinity of LT, a fully informative study would need to take careful account of the structure of the training program over a sustained period. Nonetheless a study of high level distance runners by Balsalobre-Fernandez and colleagues does provide relevant information. They recorded training, performance and salivary cortisol level in 15 high-level middle and long-distance runners from the High Performance Sports Center, Madrid, throughout a period of 10 months. The group comprised 12 men and 3 women, mean age 26.4 years, with personal bests in 1500-metres between 3:38–3:58 (men) and 4:12–4:23 (women). They rated training in three zones: zone 1 included long-distance continuous training, or interval training with long sets (4–6 km), at relatively relaxed paces; zone 2 included of intervals with sets of 1–3 km at approximately 5 K pace , likely to be moderately above lactate threshold; zone 3 included short-distance and sprint interval training at paces ranging from around 1500m pace to full sprint. Thus zone 1 and 3 roughly correspond to low intensity and high intensity zones of a polarised program, while zone 2 sessions are a little more intense but less sustained than a typical threshold training session in the mid-zone of a typical polarised program.

During the winter months, the athletes did a substantial amount of low intensity (zone 1) training. The 25 weeks of spring and summer training was dominated by zone 2 training. For 15 weeks within this 25 week period, the average training zone was in the range 1.75-2.25, indicating a large proportion of zone 2 training; while for 3 weeks the average was above 2.25, indicating an appreciable amount of training in zone 3 in addition to zone 2.

In addition to recording race performance, Balsalobre-Fernandez and colleagues regularly assessed vertical counter-move jump height (CMJ) as a measure of neuromuscular performance. Averaged over the entire season, the runners with higher long-term cortisol levels has significantly lower CMJ scores, confirming that sustained elevation of cortisol is associated with poor neuromuscular performance. However, analysis of correlations between weekly average cortisol and CMJ values revealed that higher CMJ scores were recorded in weeks with higher cortisol levels, indicating that transient elevation of cortisol is associated with better neuromuscular performance. The weeks with higher CMJ performance were weeks with lower training volume but higher training intensity (i.e. more Zone 3 sessions). Finally, CMJ scores were significantly higher in the week before the season’s best competition performance

In summary, the evidence from the study by Balsalobre-Fernadez and colleagues confirms that sustained elevation of cortisol is harmful and favours a lower volume of higher intensity training rather than moderately large volume a little above lactate threshold. This might be a key to understanding why polarised training might be superior to threshold training. In my next post, I will examine the mechanisms by which the training adaptations required for distance running might be best achieved using a polarised approach. In particular I will discuss the ability of negative ions such as phosphate and bicarbonate in the blood to provide temporary buffering of the acidity associated with lactate production. This buffering might allow transient surges of lactate produced by brief high intensity exercise to produce beneficial enhancement of the transporter molecules that facilitate transport of lactate from type 2 to type 1 muscle fibres in which it can be used as fuel, and also the transport of lactate from muscles to liver and heart, without the potentially damaging effects of increased acid levels associated with sustained increase in level of lactate.

In recent days there has been an interesting discussion on the Fetcheveryone ‘Polarised training’ thread about the value of the short intense hill sprints that Renato Canova and Brad Hudson recommend for distance runners.

Typically these take to form of 6 or more short (6-8 second) intense uphill sprints with adequate recovery between each sprint. They can be done at either the beginning or end of a training session. Canova recommends them up to twice a week. I have never done them more frequently than once per week. Although 6 hill sprints do not add greatly to the training load of a ‘serious’ athlete, I have always been concerned to avoid the risk of excessive stress. It is more important to maintain good form that promotes optimum muscle fibre recruitment

One of the immediate benefits is a feeling of speed in your legs that can make subsequent fast pace running feel relatively easy. Some athletes do intense hill sprints in the 24 hours before a race for this purpose. Although I have not habitually done this, I usually do ‘bounding’ drills during the taper for a target race to achieve a similar result. In fact hill sprints are probably safer than bounding drills as they present little risk of injury provided you warm up adequately.

I think that the feeling of ‘having speed in your legs’ is based largely on the sensation of recruiting fast twitch fibres. However, you might wonder why this is helpful for a long distance runner, since fast twitch fibres are poorly adapted for aerobic metabolism. I suspect the reason is that fast twitch fibres are good at capturing the energy of impact at footfall as elastic energy. Provided you have developed the ability to recycle lactate from fast-twitch fibres to slow twitch fibres that can use the lactate as fuel, the fast twitch contractions do not lead to increase in blood acidity.

In the past seven posts I have addressed the challenge of maximising longevity as a distance runner. For many of us, age appears to offer the prospect of inexorable decline. In contrast, a few individuals achieve performances in their 70’s or 80’s that would be a source of great satisfaction for many runners 30 years younger. Ed Whitlock recorded a time of 2:54:48 in the 2004 Toronto Waterfront Marathon at age 73 and as recently as a week ago, set an M85 half-marathon world record of 1:50:47 in the Waterloo half-marathon. Even Ed is slowing as the years pass, but he has transformed our understanding of what an elderly distance runner can achieve.

In a previous blog post I attempted to tease out the secrets of Ed’s phenomenal longevity. I concluded that his remarkably high maximum heart rate, determined largely by his genes, was one of the key elements that made him truly phenomenal, but his life-style and training allowed him to realise the potential offered by his genes. A central feature of his training has been frequent long, slow runs of up to 3 hours duration, often up to four or five times in a week. This high volume of low intensity running is augmented by moderately frequent races, typically over distances of 5-10Km.

For most of us, merely attempting to emulate Ed’s training would be impractical, either on the grounds of lack of time, or because our bodies could not cope with the volume of training. However, I believe that if we examine the anecdotal evidence provided by the training of Ed Whitlock and augment this with evidence that is emerging from current scientific studies of aging itself and of the way in which the aging body reacts to training, we can begin to formulate some general principles that will help maximise the chance of achieving the potential longevity offered by our genes. It is also encouraging that the rapid accumulation of scientific knowledge offers the prospect of even better guidance in the future.

Meanwhile I have assembled a set of 12 principles that encapsulate much of the material presented in the past seven posts. In this summary, I will not present the evidence justifying these principles. That evidence is presented in the preceding articles. Here are the 12 principles:

Continue to run regularly. The evidence indicates that continuing to run, at least into the seventh and eight decades decreases risk of disability and death. However, by virtue the stressful effect of the impact at foot-strike, and also because running tends to exacerbate the age-related shift of hormonal balance away from anabolism (building up of tissues) towards catabolism (break down of tissues), the risks associated with running are greater in the elderly than in young adults. Greater care is required to minimise these risks.

Increase training volume gradually. Gradual increase minimises the stress of training and decreases the risk of excessive rise in the stress hormone cortisol, and allows gradual building of resilient less injury-prone tissues.

Recover thoroughly after strenuous training and racing. The major reason is to ensure that acute inflammation resolves rather than becoming potentially destructive chronic inflammation. However to prevent the development of constrictive adhesions due to the deposition of collagen fibres, it is important to maintain mobility during recovery. This might be achieved by easy exercise – walking, jogging, or elliptical cross training. Perhaps stretching has a role to play though there is little compelling evidence in favour of stretching. There is substantial evidence in favour of massage.

Do a substantial amount of low intensity training. Low intensity training promotes both mitochondrial biogenesis and fat metabolism, while also building the resilience of muscles, tendons, ligaments and bones. Low intensity training enhances the ability to handle lactic acid by developing the ability to transfer lactate from fast twitch fibres into slow twitch fibres where it is consumed as fuel.

Do a modest amount of high intensity training. High intensity training helps to sustain power (the ability to deliver force rapidly) while also being an effective way to enhance the mechanism for pumping calcium back into muscles. High intensity training enhances the ability to clear lactate from muscle and transport it to other tissues such as liver where it can be utilised.

Optimise cadence. A relatively high cadence at a given pace requires a shorter stride length, thereby reducing peak airborne height (and reducing impact forces) while also reducing braking forces. Overall, potentially damaging forces are reduced. However high cadence does increase the energy cost of repositioning the swinging leg, so very high cadence is inefficient. The most efficient cadence increases with increasing pace. Most runners increase cadence with increasing pace. Nonetheless for the elderly runner, it might be best to maintain a quite high cadence during training even at low paces because minimising impact forces is more important than maximising efficiency.

Engage in low impact cross training. Although running itself is the most effective way of getting fit for running, running is a very stressful form of exercise on account of the impact forces. Many of the desired benefits of training, especially cardiac fitness, can be acquired through other forms of exercise. Low impact cross training, (elliptical, cycling, walking) provides substantial benefit with minimum damage.

Do regular resistance exercise. Resistance exercises help maintain strength and power, while promoting anabolism, thereby correcting the age-related tendency towards an excess of catabolism over anabolism. There are many different forms of resistance exercise. I do regular barbell squats and dead-lifts with quite heavy loads (typically 100Kg) and also do hang-cleans to enhance power in the posterior chain muscles (glutes, hamstrings, gastrocnemius). These exercises enhance the recruitment of type 2 fibres.

Consume a well-balanced diet. The question of the healthiest diet remains controversial, but there is no doubt that elderly individuals require a higher intake of protein to maximise tissue repair; variety, including bright coloured vegetables, helps ensure adequate intake of micronutrients. At least a moderate amount of omega-3 fats is required to promote repair of cell membranes, but a balance between omega-3 and omega-6 is probably necessary to promote acute inflammation with minimal chronic inflammation.

Get adequate sleep. Sleep is a crucial element of recovery. It promotes a naturally regulated release of growth hormone and encourages tissue repair.

Avoid sustained stress. The body is a dynamic system that requires a degree of challenge, and hence of stress, to prevent atrophy. The body responds to stress of any kind – physical or mental – by increasing release of the stress hormones, adrenaline and cortisol. In the short term this shifts the hormonal balance towards catabolism mobilising the energy required to respond to the stress, but if sustained it damages tissues, not only via break-down of body tissues, but also by promoting more subtle damage to DNA, as discussed in my post on ‘whole body factors’. To achieve well-being in life and optimum benefit from training, any stress, from whatever cause, should be accompanied by a commensurate amount of recovery. Measurements such a heart rate, heart rate variability, and blood pressure can provide useful warnings of harmful imbalance. However, our brains are very well attuned to assessing our level of stress, and sensitivity to one’s own sense of well-being also offers useful guidance.

Develop confidence in control over one’s life. Scientific evidence from large studies demonstrates that a sense of control over one’s life promotes longevity, while abundant anecdotal evidence illustrates that confidence is a key element in athletic performance. Good health and optimal performance are facilitated by minimising self-defeating thoughts. Each individual needs to develop their own strategies for achieving this.

I have been pleased to see from the stats provided by Word-press that many readers from many parts of the world read my blog. There are typically around 30,000 page views per year from over 100 different countries. I started this blog nine years ago with the aim of encouraging discussion and debate about efficient running and training. Over the years there have been some vigorous debates, mainly about the more controversial issues of running technique. The challenge of achieving longevity as a distance runner has not aroused the same passions. In part this is because the evidence is less controversial, but nonetheless, some of the evidence could be challenged, and there are many areas in which it could be expanded. Please let me know if you disagree with these principles or alternatively consider there are other important things to be taken into account.

After examining the anecdotal evidence provided by elderly marathoners and then grappling with some of the basic science underlying longevity in recent posts, it is time to attempt to draw some practical conclusions about what can be done to optimise longevity as a runner. While the unfolding science of the molecular mechanisms by which our bodies respond to wear and tear offers intriguing prospects of identifying strategies for promoting heathy aging, there are at this stage more questions than answers. However we each live only once and if we want to optimise our chances of running fluently in old age, we must make the most of the evidence that is currently available. Despite the uncertainties, the evolving science provides a framework for weighing up the value of the lessons that might be drawn from the anecdotes.

But it is necessary to be aware of the pitfalls if we are too simplistic in our interpretation of the science. For example, at first sight the fact that catabolic hormones such as cortisol promote the break-down of body tissues to provide fuel for energy generation in stressful situations, suggests that avoiding sustained elevation of cortisol is likely to promote longevity. Indeed this conclusion might be valid in some circumstances, but it is not a universal rule. The strategy that is most successful for promoting longevity in animals is a calorie restricted diet. This works for creatures as diverse as worms, fish, rodents and dogs, and there is some evidence for health benefits in primates. The mechanisms by which it achieves its benefits include an increase in resistance to oxidative damage to tissues by virtue of more resilient mitochondrial membranes. However calorie restriction is stressful and promotes long term elevation of cortisol. It appears that animals actually need at a least a moderate level of ongoing stress to encourage heathy adaptation. The goal is achieving balance between stressful stimuli and adaptive responses. The balance point depends on individual circumstances, and is likely to shift as we grow older.

The nature of training

The basic principle of athletic training is stressing the body in order to encourage it to grow stronger. One of the key mechanisms by which this is achieved is inflammation, a process by which damage to tissues generates a cascade of responses mediated by chemical messenger molecules that circulate in the blood stream, triggering repair and strengthening but also leaving a trail of debris.

There is abundant evidence that running increases life expectancy. In a 21 year follow-up study of elderly runners Chakravarty and colleagues at Stanford University found that continuing to run into the seventh and eighth decades has continuing benefits for both life expectancy and reduction of disability. Death rates were less in runners than in controls not only for cardiovascular causes, but also other causes, including cancer, neurological disorders and infections. Nonetheless, unsurprisingly, Chakravarty reported that although the increase in disability with age was substantially less in runners than in non-runners, the runners did nonetheless suffer increasing disability over the follow-up period. This is of course what would be expected if the processes by which training strengthens the body also leave a trail of debris.

If our goal is to increase not only life expectancy but also to achieve healthy aging and longevity as runners, we need to look more closely at the mechanisms by which running damages tissues. Ensuring longevity as a runner requires training in a manner that ensures that the accumulation of debris is minimised.

Healthy aging is a process affecting all parts of the body. Nonetheless, for the runner, the cardiovascular system, musculoskeletal system, nervous systems and endocrine systems are of special importance. There is a large body of evidence about how these systems age and about both the beneficial and the damaging effects of running on these systems. I will examine the evidence regarding cardiovascular system in this post, and draw some tentative conclusions about how we might train to achieve healthy aging of the heart. In my next post I will examine the evidence regarding the musculo skeletal system, for which much more detailed information about cellular mechanism is available due to the feasibility of tissue biopsy. This will allow us to extend and consolidate the conclusions regarding optimal training for maximizing longevity as a runner. In the final posts in this series I will turn my attention to the nervous and endocrine systems, and speculate about the way in which optimal training might impact upon health aging of those crucial systems.

In the medium term (over time scale of weeks) regular training leads to an increase in blood volume. This increases venous return to the heart. The stretching of the heart muscle leads to more forceful contraction and a greater stroke volume. The cardiac output for a given heart rate is increased. Resting heart rate decreases and the heart rate required to run at a particular sub-maximal pace decreases.

In the longer term, the heart muscle is remodelled, with an increase in overall volume and in thickness of the ventricular walls. This condition is known as ‘athletes heart’. The mechanism is mediated by the intra-cellular signalling pathway that engages an enzyme known as Akt, which promotes growth of both muscle cells and capillaries. This is usually regarded as a benign physiological adaptation. The enlargement of the heart that accompanies pathological conditions such as high blood pressure or obstruction of the heart valves is also mediated by the Akt signalling pathway, but in contrast to the benign enlargement of the athlete’s heart, the Akt signalling is accompanied by inhibition of a growth factor required for the development of capillaries. Thus, in the athlete’s heart the enlargement is accompanied by adequate development of a blood supply to the heart muscle, whereas in pathological conditions the blood supply is usually inadequate.

However, in some athletes the enlargement might have adverse effects. There is compelling evidence that endurance runners with a long history of substantial training have an increased risk of disturbances of heart rhythm, including both ‘supra-ventricular’ disturbances such as atrial fibrillation, and potentially more lethal ventricular disturbances. The cause of these rhythm disturbances is not fully established but it is probable that the re-modelling of the heart muscle in a way that alters electrical conduction pathways plays a role. It is likely that residual fibrosis at sites where damaged muscle has been repaired also plays a role by producing local irritability of the cardiac muscle cells leading them to fire spontaneously.

During intense prolonged exercise the strength of ventricular contraction, especially that of the right ventricle, is diminished, a condition known as Exercise-Induced Right Ventricular Dysfunction. If the exercise is sufficiently intense and prolonged, cardiac enzymes can be detected in the bloodstream, indicating a least temporary structural damage to heart muscle.

In a study of forty highly trained athletes competing in events ranging from marathon to iron-man triathlon, LaGerche and colleagues from Melbourne found transient weakening of the right ventricle immediately after the event. This was more severe the longer the duration of the event. The transient weakness returned near to normal within a week. However in 5 of the athletes, there was evidence of long term fibrosis of the ventricular septum, indicating chronic damage. Those with evidence suggesting long term damage had an average age of 43 and had been competing for an average of 20 years. Those without evidence of chronic damage had an average age of 35 and had been competing for an average of 8 years. The evidence suggests that duration of endurance competition is a strong predictor of chronic damage.

Although an enlarged athlete’s heart usually has a much better blood supply than the enlarged heart associated with high blood pressure or obstruction of the heart valves, there is disconcerting but controversial evidence of excessive calcification of the arteries in at least some athletes, especially in males in who run marathons over period of many years. The mechanism is uncertain, though sustained inflammation is a plausible mechanism.

Effects of the amount and type of training

Although an overwhelming mass of evidence demonstrates that runners have a longer life expectancy and in particular, a lower risk of death from heart attack or heart failure than sedentary individuals, several large epidemiological studies raise the possibility that adverse health effects (especially cardiac events) tend to be a little more frequent in those who engage in a large amount of exercise than in those who exercise moderately. The US Aerobic Longitudinal Study examined the associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, aged 18 to 100 years (mean age 44 years) over an average period of 15 years and found a marked decreased in both cardiac and all-cause mortality in runners compared with non-runners, but the reduction in mortality was a little less in those training 6 or more times per week compared with those training 1-5 times per week. The Copenhagen City Heart Study followed 1,098 healthy joggers and 3,950 healthy non-joggers for a period of 12 years and found that 1 to 2.4 hours of jogging per week was associated with the lowest mortality. These ‘moderate’ joggers had a mortality hazard ratio of 0.29 compared with sedentary non-joggers.

But closer look at the evidence reveals a potentially informative detail. In a study of heart health of over a million women, Miranda Armstrong and her co-investigators from Oxford found that among obese women, those who did a large amount of exercise suffered more heart problems than those who did a moderate amount. However, in contrast, among the women who had a Body Mass Index less than 25, those doing a large amount of exercise had fewer heart problems than those doing a moderate amount of exercise. This suggests that if there is a risk in doing a large amount of exercise, it is mainly confined to those for whom the exercise is excessively stressful due to other risk factors that shift the balance towards harm rather than benefit.

Although the evidence from the large epidemiological studies remains a topic of debate because of issues such as possible bias in participant selection and the relatively small numbers of individuals in the category who take a very large amount of exercise, I think the balance of evidence does indicate that at least some individuals who take a large amount of exercise do have an increased risk of death, including death form cardiac events, within a given time period. In my opinion, the important question is what determines which individuals will be harmed by a large amount of exercise, and whether there are ways in which we can minimise the risk of harm.

There is evidence that adequate prior training can protect against damage. Neilan and colleagues studied non-elite marathoners runners completing the Boston Marathon and reported that right ventricle weakness was more pronounced in those who had trained less than 35 miles per week compared with those who had trained more than 45 miles per week. The logical conclusion from studies such as the Oxford study of obese female runners and Neilan’s study of marathoners is that running in a manner that exceeds the individual’s current ability to cope with the stress increases the risk of damage. This in turn suggests that building up gradually in a manner that ensures that training sessions are never excessively stressful is likely to be the safest approach.

Furthermore, it is likely that lack of adequate prior training or obesity are not the only factors that impair the ability to cope with the stress of demanding training and racing. Following a very demanding marathon or ultra-marathon, the evidence of damage remains detectable for a period of weeks. It is plausible that demanding training when the heart is in a weakened state will compound the damage. It is widely accepted in practice that recovery following intense racing or heavy training is crucial, but unfortunately there is relatively little scientific evidence addressing the question of whether or not the adverse cardiac effects of intense exercise resolve during a recovery period, or conversely, whether the adverse effects are compounded by repeated bouts of exercise. We must therefore turn to evidence from studies of rats.

Benito and colleagues exercised rats on a treadmill for 60 minutes at a quite vigorous pace of 60 cm/s (achieved after 2 weeks of progressive training) 5 days per week for a total of 4 weeks, 8 weeks or 16 weeks. For a rat, 16 weeks of life is roughly equivalent to 10 years for a human. During the first 8 weeks there was relatively little evidence of damage, but prominent signs of damage emerged between 8 and 16 weeks. After the 16 weeks of exercise, the rats exhibited hypertrophy of the left ventricle and also the reduced function of the right ventricle, similar to the findings reported in humans. Furthermore the rats had marked deposits of collagen in the right ventricle, and messenger RNA and protein expression characteristic of fibrosis in both atria and the right ventricle. The exercised rats had an increased susceptibility to induction of ventricular arrhythmias. A sub-group of the rats were examined after an 8 week recovery period following the 16 weeks of exercise. Although the increased weight of the heart had not fully returned to normal level, all of the fibrotic changes that had been observed after 16 weeks of exercise had returned to the normal level observed in sedentary control rats. Thus, at least in rats, the adverse potentially arrhythmigenic changes produced by intense exercise over a 16 week period appear to be reversible after an adequate recovery period. Thus the best available scientific evidence does support the accepted principle that recovery following intense racing or heavy training is crucial.

Proposed cardiac outcomes of long-term training. The size of the ellipses indicates cardiac fitness at each stage; colour indicates balance between recovery (blue) and stress (red)

In summary, the evidence regarding the cardiovascular effects of running suggests the following guidelines for healthy aging and longevity as a runner:

Continuing to run regularly, at least into the seventh and eight decades decreases risk of death and disability.

Training volume should be built up gradually.

Adequate recovery after demanding events, such as a marathon (or indeed, even after heavy training sessions) is likely to be crucial.

My next post will examine the evidence regarding the effects of training on the musculoskeletal system, and will both consolidate and extend these conclusions.

Over the past two years I have written on several occasions about the training of Ed Whitlock, without doubt the greatest elderly distance runner the world has ever seen; the first and only 70 year old to run a marathon in less than 3 hours and holder of the age-group world marathon records for ages M70-74, M75-79 and M80-84, together with the M80-84 world records for 1500m, 3000m, 5Km, 10Km, 15Km and half-marathon, and numerous other records. While may factors, including genes for longevity and intense training in early middle age probably contribute to this phenomenal ability, the striking feature that sets him apart from all others is his approach to training: he runs for up to 3 hours per day at a slow pace, many days a week, and in addition, races fairly regularly over distances ranging for 3000m to 10,000m. His overall training program can be regarded as the ultimate in polarised training.

Whitlock himself makes no special claims for his training, other than noting that it works for him. Apart from having an uncle who lived to age 107, there little that is remarkable about his background or his physiology that might explain his phenomenal distance running ability. When assessed at age 70 he had a VO2 max that was high for a man of his age, but consistent with his running performance. A high VO2 max might be a consequence of training and/or genes.

The fact that he won the M45 world masters 1500m championship in 4:09 at age 48 makes it likely that his VO2max was already relatively high very early in middle-age. At that stage his training included a substantial number of intense track sessions. It is therefore unlikely that his VO2max at age 70 can be attributed entirely to the nature of the training and racing that he has done since his late 60’s.

He has maintained this polarised pattern for more than 15 years, apart from several instances in which misadventure or injury have demanded quite long periods of recovery, during which he has re-built training volume slowly. Whatever the contributions of his genes and the training earlier in his career, the long duration of his current pattern of training and racing does indicate that this current pattern has succeeded in maintaining his extremely high level of performance into his mid-eighties. It is therefore potentially worthwhile for other elderly distance runners to explore the possibility that it might work for them.

About 18 months ago, I set out to emulate the major features of his training program, aiming for at least three long slow runs each week, gradually increasing the duration from 60 minutes to 120 minutes over a period of 3 months. As I still work and have limited time available, I was obliged to do two of my long runs on the week-end and therefore had little opportunity for the intense racing that was part of Ed’s program. I was also aware of the need to avoid placing undue stress on my left knee that had bene damaged in an episode of acute arthritis a few years ago. I therefore replaced Ed’s intense racing with intense sessions of 30-50 minutes duration on the elliptical cross trainer.

Over a three month period I was able to build up the duration of long runs with no difficulty. I enjoyed not only a clear increase in endurance but also developed a substantial capacity to metabolise fat, most noticeable from my ketotic breath at the end of long training runs. However the improvement of my aerobic capacity, assessed by calculating beats/Km recorded over similar terrain, was only modest. I was a little disappointed by this modest gain, and also a little disconcerted by early signs of accumulating fatigue in December. Nonetheless, I considered that progress at that stage was satisfactory, and was looking forward to a spring marathon.

However a problem that I should have foreseen developed over the winter. I have long standing asthma that is usually relatively mild, though it is exacerbate by cold air. I also tend to suffer from various side effects of my asthma medication, and have had little success form changing to different medications. I therefore need to limit the dose. Inhaling cold winter air for periods of several hours during my long runs triggered marked constriction of my airways. To add to this, beginning in mid-December, I suffered a series of quite severe upper respiratory tract infections that exacerbated my breathing difficulties. I was forced to defer my Whitlock style training until the spring. By March my fitness had deteriorated quite markedly. Once again I began the gradual build-up of long run duration. Progress was slow, but nonetheless, I set my sights on an autumn marathon.

During a long run in the Borders District of Scotland in April with my marathon running sister-in-law, Mary, who took the photos

Like Ed Whitlock in training, I adopted a short stride and high cadence to minimise impact damage to my legs.

Then in July disaster struck. I suffered quite a nasty fall from my bicycle when the front wheel got stuck in tram–tracks that I need to cross at an oblique angle on my daily commute to work. I hit the ground very hard, producing spectacular bruising at every protruding point on the right hand side of by body from knee to forehead. For several weeks, one side of my face was stained, at first purple and then yellow, along the path where a broad tide of blood had tracked beneath the skin. The initial concern of the two nurses who rushed to my aid at the scene of the fall had been the possibility of serious head injury, but in the longer term, after the bruises had faded, it turned out that the most troublesome injuries were to my left knee and right elbow. I had torn lateral ligaments of my left knee, and also damaged the attachment of tendons at my right elbow. Even now, five months later, both of these injuries limit my movements. The physio anticipates it will be a year before the knee has recovered.

For several months I could not run at all, but over the past two months I have been cautiously rebuilding once again. In recent weeks I have increased the length of my ‘longish’ runs up to 10Km. The most dismaying feature is that I cannot cope with paces any faster than 10 minutes/mile. While the crucial limitation is the knee, I am also appalled by how unfit I have become. I remind myself that Ed Whitlock has on several occasions taken almost year to get back to fitness after an injury. In fact Ed has scarcely raced at all this year, subsequent to an upper thigh/ groin injury that he suffered last year. For two successive years he has missed the Toronto Waterfront Marathon – an event in which he had set a single age world record on six occasions during the preceding decade. However, despite failing to be on the starting line for this year’s marathon, he did set an M84 single age 10K World Record of 49:08 in the Longboat Island Race in September.

I have no expectation of setting any records, but I fear that even after making generous allowance for the expected slow recovery from my illness last winter and my injury in the summer, I am suffering an alarming deterioration in my overall physical condition. I suspect that I do not have good genes for longevity. In my next post I will examine the evidence regarding genes for healthy aging.

But whatever my prospects for the longer term future, I am now focused on rebuilding my endurance. Despite the limited evidence that a Whitlock style program is the best way for me to build aerobic fitness, my experience so far does indicate that it is a good way to build endurance. As this is my immediate goal, I am again using a modest version of a Whitlock style program. At present, three runs per week, each of an hour in duration, is about all my body can cope with. Promoting recovery of my knee ligaments and also vigilant deployment of my inhaler to minimise the constriction of my airways during winter training runs will be equally high priorities. I will not set any marathon target for the near future. I am playing with the idea of setting targets for a ’heptathlon’ of physical activities, including not only running but also some other challenges to be completed in the week of my seventieth birthday in March. I will defer specifying the specific targets until I establish how my recovery progresses in December.

It is well established that countermove jump height (CMJ) is a good predictor of sprinting speed. This is not surprising because CMJ performance depends on powerful type 2 muscle fibres and on the ability to coordinate the recruitment of these fibres. In the CMJ, flexion of the hips and knees produces eccentric contraction of the corresponding extensors immediately prior to the explosive concentric contraction that propels the body upwards. It is necessary to recruit the muscle fibres in a manner that harnesses the enhancement of power generated by the eccentric contraction.

The relationship between CMJ performance and distance running performance has been less thoroughly investigated.

In assessing endurance training, aerobic capacity and lactate threshold have been the main foci of attention, but other training-related variables also predict performance. It is has been demonstrated that difference between elite athletes in volume of zone 1 training (comfortably below LT) predicts distance race performance (e.g. 10Km). In addition, it is fairly well established that a high values of the ‘stress hormone’ cortisol sustained across a period of months predicts poorer performance.

However, somewhat paradoxically, within an individual athlete, week to week variations in training volume and cortisol values make the opposite predictions. In a study comparing seasons best and seasons worst performance in elite athletes, total training volume was less but volume of zone 3 training (appreciably above LT) was greater in the week before the seasons best performance. Cortisol tended to be higher a week before the best performance, Countermove jump height was also higher in the week before the best performance.

This apparent paradox is consistent with the evidence that a taper should involve decrease volume but not a decrease in training intensity. The fact that CMJ was higher before the season’s best performance suggest to me that zone 3 training in the week preceding the event promotes good neuromuscular coordination.

The importance of neuromuscular coordination is clearly illustrated by the clunkiness that triathletes experience during the bike to run transition. The rapid gains in weight lifting performance at the beginning of a lifting program are most likely due to improved recruitment of muscle fibres. Conversely, fatigue impairs neuromuscular coordination, and measurement of postural sway has been proposed as a sensitive measure of impaired neuromuscular coordination arising from fatigue in footballers.

Overall, the evidence indicates that neuromuscular coordination is crucial for both athletic performance and injury minimization but it is rarely the focus of attention in endurance training. While not a specific focus of attention, when we engage in routine warm up we do in fact achieve short-term enhancement of neuromuscular coordination, and when we accumulate miles of training, we engage in long-term enhancement of neuromuscular coordination, but we rarely think of these activities as exercises in enhancing neuromuscular coordination. However, we are more likely to produce effective enhancement of neuromuscular coordination if we plan our warm-up and training activities bearing neuromuscular coordination in mind.

The elements of coordination

Recruitment of the optimal number and type of muscle fibres: because much of our training should be at an intensity less than racing intensity, we need pay attention to the need to ensure that we do retain the ability to recruit type 2 fibres as effectively as required at race pace. Although the importance specificity in training is sometimes over-rated, at least some specificity is essential. As discussed in my recent post on lactate shuttling, beneficial enhancement of the ability to handle the accumulation of the lactate can be achieved by a large volume of low intensity training. However the danger of a program focussed too strongly on low intensity running is the development of a tendency to plod slowly under all circumstances. It is therefore crucial to do at least some training at or near race pace, especially when fatigued as is likely to be the situation in the later stages of a race. Progressive runs that achieve a pace at or even a little faster than race pace are likely to be beneficial

Recruitment of muscles in the optimal sequence: The action of running entails a very complex combination of muscle contractions, requiring that the extensors and flexors at each of the major joints of the leg are recruited in a precisely timed sequence.

Speed of recruitment of muscle fibres: With increasing age, deterioration in running speed is associated with loss of stride length; not cadence. This is accompanied by a atrophy of muscles and loss of strength. However as I found three years ago when engaged in intense high-load weight lifting program for several months, I was able to increase my strength to the point where I could squat a heavier load than Mo Farah, but my stride length did not increase appreciably, and my speed remained but a very pale shadow of Mo’s speed. Speed depends on power: the ability to exert force rapidly. This requires effective, rapid recruitment of muscle fibres. It is far harder to train power than speed, though there is some evidence that focussing on a rapid contraction during the concentric phase of a lift, at moderate load, can produce a worthwhile gain in power.

Implications for warming up For most of my training sessions, I employ a warm up procedure that includes 10 activities, beginning with simple movements designed to get all of the major joints of the leg moving freely, and proceeds though a sequence in which power output gradually increases.

Calf raises

Hip swings, (straight front to back; rotating from foot behind to opposite side in front.)

Body-weight squats (aiming for hips below knees)

Single leg squats

Lunge, to front and side

High knees

High knees skipping

Hopping (fast, small hops)

Jogging

Surges at race pace

Time for each is adjusted according to how my body is reacting, though typically each of the first 8 activities takes 20-60 seconds; the focus is on fluent action rather than effort.

Implications for injury minimization Recent studies, reviewed by Herman and colleagues, reveal that in a variety of different sports, poor neurocognitive performance, either at baseline or in the aftermath of a concussion, is associated with elevated risk of musculoskeletal injury. It is probable that a thorough warm-up that sharpens up neuromuscular coordination is a good way to minimise risk of injury.

Measuring neuromuscular coordination The CMJ is widely used in various sports, especially team games such as football, to assess fitness. However, it has three potential disadvantages as a measure of neuromuscular coordination for the distance runner: 1) it is not a ‘pure’ measure as performance depends on type 2 fibre strength in addition to coordination; 2) maximal performance is quite demanding and creates the risk of injury; 3) accurate measurement requires special equipment.

I have been experimenting with time taken to perform 20 line jumps as a test of coordination. It does depend on other aspects of fitness such as muscle strength to at least a small extent, but placing the emphasis on time rather than maximal power focuses attention on coordination rather than strength. The risk of injury is small. At this stage, the utility of timed line-jump performance as a test remains speculative as I have not tested it systematically. Typically, I find that my time for 20 line jumps decreases from 9.0 seconds after a few minutes of jogging to 7.5 seconds after the ‘neuromuscular’ warm up described above. Time for 20 jumps increases dramatically after a long run. Provided I can establish that the test yields consistent results when assessing deterioration in neuromuscular coordination associated with fatigue, I plan to use it to determine whether or not light weight shoes (Nike Free 3.0) result in greater deterioration in coordination during a long run, compared with more heavily padded shoes.

Conclusion It is almost certainly true that many of the activities that athletes and coaches have traditionally incorporated into warm-up and training achieve their benefit at least partly through enhancing neuromuscular coordination. However by focussing on the more easily quantifiable physiological variables when planning and assessing training sessions, there is a risk that endurance athletes might fail to optimise training to achieve the required combination of aerobic capacity, strength and coordination. Perhaps we should place more emphasis on a systematic approach to enhancing neuromuscular coordination during training, and on measuring it to assess the outcome of that training.

Races from 5000m to marathon are run at a pace that is strongly predicted by pace at lactate threshold because the accumulation of acidity is a major factor limiting muscle performance. During the combustion of glucose to generate energy, the major source of acid is lactic acid. Lactic acid is a compound of two ions: negatively charged lactate ions and positively charged hydrogen ions. Under normal circumstances within the body, lactic acid dissociates into these two constituent parts, lactate and hydrogen ions, and it is the latter that create the acidity. At least in part, the hydrogen ions are buffered (i.e. mopped-up by other negative ions within tissue) but once this buffering capacity is saturated, hydrogen ions accumulation creates an acid environment that impairs the efficiency of muscle contraction.

However lactate itself can be used as fuel in various locations in the body, and as it is itself metabolised hydrogen ions are removed. Thus, understanding the mechanisms by which lactate is transported around the body and the mechanisms by which it is itself metabolised provides the basis for rational planning of training.

The orthodox view

The scientific studies of Louis Pasteur, in the nineteenth and early twentieth century, and subsequently by Hans Krebs, AV Hill and others, early in the twentieth century uncovered the mechanisms of anaerobic and aerobic metabolism of glucose, and established the orthodox view that shaped the theory of training for distance training through the second half of the twentieth century. According to this orthodox view, glucose is initially metabolized by the process of glycolysis, to produce pyruvate, This anaerobic transformation of glucose to pyuvate releases a modest amount of energy which is transferred into the high energy bonds of the energy-rich molecule, ATP, and ultimately can be used to fuel muscle contraction. But in the presence of oxygen much more energy can be derived via aerobic metabolism of pyruvate. The pyruvate is transported into mitochondria and converted to acetyl-CoA by an enzyme complex known as the pyruvate dehydrogenase complex. Acetyl-CoA then undergoes a series of chemical transformations catalysed by the aerobic enzymes within mitochondria. The acetyl group is oxidized to carbon dioxide, releasing a relatively large amount of energy which is incorporated into ATP, thereby providing a substantial enhancement of the supply of energy for muscle contraction. In contrast, when the rate of delivery of oxygen to muscle is inadequate, muscle contraction must be fueled via the modest energy yielded by conversion of glucose to pyuvate, and the pyruvate is converted to lactate, thereby generating potentially harmful acidity.

The lactate shuttle

The orthodox view is indeed substantially correct, but is misleading because a substantial proportion of pyruvate is converted to lactate even when oxygen supply is adequate to sustain aerobic metabolism in mitochondria. The way in which the body deals with this lactate is of crucial importance to coaches and athletes. It was not until the final years of the twentieth century that an adequate understating of the way in which lactate in handled in the body emerged. The newly emerging understanding was based largely on the work of George Brooks of the University of California, Berkeley Campus, who developed the concept of the lactate shuttle. Lactate shuttling refers to a group of processes by which lactate is transported within and between cells to locations where is undergoes metabolism. There is still debate about the details of these mechanisms but the broad principles are now clear, and these principles have major implications for optimum training for distance running.

The first key point is that a proportion of the pyruvate generated in the first stage of glucose metabolism is converted to lactate in the cytosol (the fluid medium inside cells) of muscle fibres, across a very wide range of work-rates, extending from the low aerobic to anaerobic zones. In the low and mid-aerobic range, the majority of the lactate is transported across various membranes to various different sites where it is metabolized, so there is very little observable accumulation of lactate in blood until the rate of generation of lactate rises near to the limit of the body’s ability to transport and utilize lactate. Beyond this point, the concentration of lactate and hydrogen ions in blood rises rapidly (the Onset of Blood Lactate Accumulation, OBLA); respiration becomes very effortful, and the ability to maintain that pace is limited by the limited ability to tolerate acidity.

It is helpful to understand the various processes by which lactate is transported out of the cytosol of muscle cells and subsequently metabolized, in order to design a training program that is likely to enhance these processes.

There are four major pathways by which lactate is transported and metabolized:

Transport across the outer mitochondrial membrane to a site where lactate dehydrogenase converts lactate back to pyruvate which then undergoes aerobic metabolism within the same muscle cell. This process results in dissipation of lactate and acidity in the cell where it was created and hence is merely a mechanism that ensures that acid does not accumulate when oxygen supply is adequate to sustain aerobic metabolism.

Transport out of the muscle fibre where it was created, into nearby fibres where is can be transported across the outer mitochondrial membrane and metabolized. This mechanism makes it possible for lactate to be generated in type 2 muscle fibres, which are powerful but have relatively low aerobic capacity, and then metabolized in type 1 fibres which have high aerobic capacity. Training ‘at a good aerobic pace’ as advocated by Lydiard is potentially a good strategy for developing this mechanism. Although the training pace might be comfortably below OBLA, the ability to dissipate lactate and acidity will be enhanced, leading to a an increase in pace at OBLA and improved performance over distances from 1500m to marathon.

Transport out of the muscle fibre where it was created into the blood and thence to other organs, such as heart and brain where it can be metabolized to generate energy

Transport out of the muscle fibre where it was created into blood and thence to liver where it can be converted back to glucose by the process of gluconeogenesis. This mechanism is likely to help conserve glucose stores in a manner that is useful in long events such as the marathon.

It is important to note that all of these processes entail transport across a membrane or several membranes prior to metabolism. Transport is an active process that is performed by specialised proteins known as monocarboxylate transporters (MCTs). There are several different type of MCT located in different types of membrane. Like many proteins in the body, utilization encourages production of increased amounts of the protein.

Aerobic base-building

Low intensity running is not merely about developing the capillaries to deliver blood to muscle and mitochondrial enzymes that perform aerobic metabolism. Because appreciable amounts of lactate are produced, transported and metabolized even at work-rates well below OBLA, low intensity training helps build capacity to handle lactate.

Think of the flow of glucose into the energy metabolic pathway as being like water flowing from an inflow pipe into a sink. The inflow pipe is actually the anaerobic pathway (glycolysis). A pool of interchangeable pyruvate and lactate tends to accumulate in the sink. There are two ways out of the sink: transport out of the cell or down the plug hole into mitochondria where aerobic metabolism occurs. In fibres in which the aerobic system has been well developed , the flow down the plughole can accommodate a large flow of glucose into the system without the sink overflowing. Shuttling from type 2 fibres which have less well developed aerobic capacity, into nearby type 1 fibres also helps maintain the flow. There is minimal accumulation of acid in either muscle or blood. So purely aerobic development, which can be achieved by low intensity training, minimizes accumulation of acid at 10K and 5K pace. Shuttling explains why runners who only do low intensity running during base building nonetheless usually find that 10K and 5K pace improve despite doing no training near race pace.

The important conclusion for the endurance athlete is that low intensity training is an effective way to develop an aerobic base which helps raise lactate threshold. It enhances performance at all distances for 1500m to ultramarathon.

Interval training and fartlek

Lactate shuttling also provides an explanation for the effectiveness of interval training and fartlek. A brief intense effort epoch above threshold generates a surge of lactic acid, and is followed by a recovery epoch during which lactic acid levels fall rapidly, before the sequence of effort and recovery is repeated. Thus, large gradients in lactate concentration develop, resolve and develop again. It is noteworthy that the drop in lactate during recovery is likely to be facilitated by low intensity running which maintains transport and utilization of lactate during recovery. A high lactate gradient across a membrane makes high demand on the transport process and is likely to stimulate production of the relevant transporters, the MCTs.

It is plausible that this will be achieved most effectively by ‘cruise’ intervals of the type employed by Emil Zatopek, or by fartlek sessions in which intensity is high enough during the effort epochs to ensure substantial production of lactate, while intensity during the recovery epochs is adequate to ensure transport and utilization of the lactate produced during the preceding effort epoch

Conclusion

The various pathways by which lactate is transported out of the muscle cells where it is created to locations where it can be usefully metabolized provide a set of mechanisms by which either low intensity training at a pace comfortably below lactate threshold, or by interval training in which lactate is generated in brief surges, can develop the ability to cope with lactate production at race pace. Thus training for sustained periods at or near race pace, which tends to be quite demanding by virtue of the sustained stress, has only a relatively limited role to play in training for endurance events. This might be an explanation for the observation that many elite endurance athletes adopt a polarized approach to training, in which the majority of training is done at a pace comfortably below threshold, together with an appreciable minority of training at higher intensity during interval sessions and a modest amount of sustained running near to threshold.